Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study
Identifieur interne : 000411 ( Istex/Curation ); précédent : 000410; suivant : 000412Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study
Auteurs : R. Nandhagopal [Canada] ; L. Kuramoto [Canada] ; M. Schulzer [Canada] ; E. Mak [Canada] ; J. Cragg [Canada] ; Chong S. Lee [Canada] ; J. Mckenzie [États-Unis] ; S. Mccormick [Canada] ; A. Samii [États-Unis] ; A. Troiano [Canada] ; T. J. Ruth [Canada] ; V. Sossi [Canada] ; R. De La Fuente-Fernandez [Canada] ; Donald B. Calne [Canada] ; A. J. Stoessl [Canada]Source :
- [ 0006-8950 ]
Abstract
Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BPND(t) or Kocc(t) ae(btdA) c, where BPND tracer binding potential (nondispaceable), KOCC tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.
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DOI: 10.1093/brain/awp209
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Sossi</name><affiliation wicri:level="1"><mods:affiliation>4 Department of Physics & Astronomy, University of British Columbia, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, Vancouver, BC V6T2B5 Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>4 Department of Physics & Astronomy, University of British Columbia, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, Vancouver</wicri:regionArea></affiliation></author><author><name sortKey="De La Fuente Fernandez, R" sort="De La Fuente Fernandez, R" uniqKey="De La Fuente Fernandez R" first="R." last="De La Fuente-Fernandez">R. De La Fuente-Fernandez</name><affiliation wicri:level="1"><mods:affiliation>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver, BC V6T2B5 Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver</wicri:regionArea></affiliation></author><author><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B." last="Calne">Donald B. Calne</name><affiliation wicri:level="1"><mods:affiliation>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver, BC V6T2B5 Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver</wicri:regionArea></affiliation></author><author><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A. J." last="Stoessl">A. J. Stoessl</name><affiliation wicri:level="1"><mods:affiliation>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver, BC V6T2B5 Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Pacific Parkinson's Research Centre, University of British Columbia & Vancouver Coastal Health, Vancouver</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: jstoessl@interchange.ubc.ca</mods:affiliation><country wicri:rule="url">Canada</country></affiliation></author></analytic><series><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Parkinson's disease is a heterogeneous disorder with multiple factors contributing to disease initiation and progression. Using serial, multi-tracer positron emission tomography imaging, we studied a cohort of 78 subjects with sporadic Parkinson's disease to understand the disease course better. Subjects were scanned with radiotracers of presynaptic dopaminergic integrity at baseline and again after 4 and 8 years of follow-up. Non-linear multivariate regression analyses, using random effects, of the form BPND(t) or Kocc(t) ae(btdA) c, where BPND tracer binding potential (nondispaceable), KOCC tracer uptake constant a, b, c and d are regression parameters, t is the symptom duration and A is the age at onset, were utilized to model the longitudinal progression of radiotracer binding/uptake. We found that the initial tracer binding/uptake was significantly different in anterior versus posterior striatal subregions, indicating that the degree of denervation at disease onset was different between regions. However, the relative rate of decline in tracer binding/uptake was similar between the striatal subregions. While an antero-posterior gradient of severity was maintained for dopamine synthesis, storage and reuptake, the asymmetry between the more and less affected striatum became less prominent over the disease course. Our study suggests that the mechanisms underlying Parkinson's disease initiation and progression are probably different. Whereas factors responsible for disease initiation affect striatal subregions differently, those factors contributing to disease progression affect all striatal subregions to a similar degree and may therefore reflect non-specific mechanisms such as oxidative stress, inflammation or excitotoxicity.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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